Discontinuous total parenteral nutrition prevents postischemic mitochondrial dysfunction in rat liver

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Abstract

Although discontinuous total parenteral nutrition (d-TPN) has recently been favored for clinical use over continuous total parenteral nutrition (c-TPN) to ameliorate liver dysfunction, mechanisms for the protection against postoperative liver dysfunction remain unknown. This study aimed to examine differences in mitochondrial function in d-TPN- and c-TPN–pretreated livers during ischemia-reperfusion. Rat livers pretreated with d-TPN or c-TPN were perfused with Krebs-Ringer buffer and were exposed to 25% low-flow hypoxia followed by reperfusion. Intrahepatic mitochondrial membrane potential (▵Ψ) and cell viability were assessed by dual-color digital microfluorography using rhodamine 123 (Rh123) and propidium iodide (PI), respectively. In response to hypoxia, livers pretreated with c-TPN, d-TPN, and an ordinary chow diet exhibited a significant ▵Ψ reduction among the entire lobules. Upon reperfusion, the regional ▵Ψ values further decreased in the c-TPN liver, whereas those in the d-TPN–treated or chow-treated livers displayed a rapid recovery toward the control levels. The severity of cell injury did not differ among the groups, showing that the reperfusion-induced ▵Ψ drop in the c-TPN–pretreated liver is not a consequence of cell injury. Differences in the ▵Ψ drop among the groups appear to occur irrespective of those in the glycogen storage, because the livers undergoing d-TPN display a marked ▵Ψ recovery even when reperfused at the end of a fasted state. These results indicate that c-TPN, but not d-TPN, jeopardizes mitochondrial re-energization and suggest that a circadian pattern of the TPN serves as a potentially beneficial strategy to reduce the risk of postischemic mitochondrial dysfunction in the liver.

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